This article is very seriously misleading and
needs to be retracted. It starts with an assertion of a highly dubious
massively important controversial “fact” with no citation whatsoever in support.
The opening sentence (of both abstract and text) asserts to us that as of
2014-15, 1% of 10-year-olds are autistic, and 1% of 30-year-olds are autistic,
1% of 50-year-olds are autistic, and so on, for “all ages”. And the title of the
paper reinforces that untruth with its fictional notion that there is (by
implication "therefore") a “lost generation” of older autistics who have mostly
remained unrecognised as autistic and thus “lost”. The un-explicated implication
being that there has not been any increase of autism but instead only an
increase of awareness or diagnosis. And this paper sets out from its beginning
by grossly misleading the reader into assuming that that is known to be a fact,
indeed established to such an extent it doesn’t even need any citation in
support.

And that title and first sentence
are not incidental to the paper but are its central premises.

I sent emails to the authors, querying the justification for that first
sentence. I got no reply from SBC, not even after I posted the letter attached
herewith to him by Signed-For delivery (KP597377771GB at www.royalmail.com, received 12th Jan
2016).[I will append that letter to end of this blogpost.]

Dr Lai sent a series of replies. The full correspondence is too lengthy to
include here in full, but here are the main elements.

His first reply was as follows (and note
furthermore the absurd sentence I have bolded, which effectively concedes my
objection anyway).

Dear Robin,

Thank you for your message. For clarification, when we
write “Autism spectrum conditions (panel 1) comprise a set of neurodevelopmental
syndromes with a population prevalence of 1% across all ages.” we are NOT
referring the term “ages” to different chronological years (i.e., 1970s, 80s,
90s, etc.) but are referring it to the ages of the individuals; that is, we are
referring to epidemiological evidences that recent cross-sectional studies in
children, in teenagers and in adults all tend to show a prevalence around 1%
(depending on studies but can range from around ~0.5% to ~2%). We,
therefore, have no intention to argue in the paper whether the prevalence of
autism is constant or not across different chronological years.

Hope this clarifies the question/mis-understanding.

Regards,

Meng-Chuan

In reply I pointed out that
this entailed an obvious absurd fallacy.

"..... Your phrase “all ages” includes obviously those who
are 40 or 60 years old. And even older. As of 2015, a person who is age 40 was
necessarily born in 1975 or earlier, and a person of age 60 was necessarily born
in 1955 or earlier. That is, such ages of persons are impossible to disentangle
from the huge change of apparent incidence (per birth-year cohorts) which is the
basis of the notion of the autism increase. I fail to see any way you can
separate ages (of “all ages”) from specific years of birth.

In response to my request for any evidence to support that
claim of your first sentence, you didn't send any, but instead included a
sentence contradicting it. And that notion of “1% across all ages” is
fundamental to the point of your entire article, namely the notion of a “lost
generation” of older autistics."

In further correspondence, Dr
Lai resolutely held to his bizarre notion that persons' ages (as of 2014-5)
could be separated from their dates of birth of after or before 1975 or
earlier. And meanwhile no reply at all has been forthcoming from Dr
Baron-Cohen.

The notion that there has been
no real increase of autism has been rejected by many people well-qualified to do
so, not least people with many years direct experience of the field such as
Bernard Rimland (founder of ARI), Prof. Sally Rogers of MIND, and Lisa
Blakemore-Brown. And the careful analysis by Hertz-Picciotto and Delwiche
concluded that the increase must be very real indeed: https://www.ncbi.nlm.nih.gov/pubmed/19234401 discussed
at:

And yet this Lancet "review"
opens its abstract and main text with a sentence which fails to even mention the
existence of that H&D 2009 paper (or anything else of the many voices
challenging their major assertion). Why no such mention? Failing to cite major counter-evidence is the hallmark
of charlatanism rather than of anything worthy to be published in a Lancet
journal. Why no reply from SBC, and only infantile nonsense from the other
author? How about because there is no sensible, honest defence for this
outrageously deceiving article. Its continuing presence unchallenged in your
journal threatens to bring your journal into disrepute too.

Sloppy, dishonest work in high places such as this "review"
undermine not only the credibility of your journal but of the medical research
community more generally. It needs to be cut out promptly rather than allowed
to remain festering.

Sincerely,

Robin P Clarke

(PS. The authors might wish
to attempt a defence on the grounds that Brugha et al. "prove their thesis
right". But (apart from the other objections above) Brugha et al. is
fundamentally unsound. They described in considerable detail their procedures
for establishing reliability of the assessments. But not a single word
about establishing of the (infinitely more important) validity of the
assessments, that is establishing that the measures at age x were equivalent to
the measures at age y. And that is because it is logically impossible to do
that validity verification (except maybe over several decades). It's a bit like
if I put a steel ruler in a hot fire and declared that I can see that its own
scale shows it to be still exactly 12 inches long, so “therefore” the heating
hasn't changed its length. Furthermore the Brugha study has been damningly
criticised for other defects as in the following quotations.

https://childhealthsafety.wordpress.com/2011/08/19/autism-figures-existing-studies-shows-shocking-real-increase-since-1988/"[The latter is not a particularly inspiring piece of work. Brugha did
not find a single adult with childhood autism, nor did he refer to Baird or
Baron Cohen but baldly claimed for comparison a childhood figure of 1 in 100,
and he changed the standard diagnostic criteria to catch adults who would not
normally have a diagnosis. Of the 14,000 potential participants there was a 50%
drop out rate with 7000 responding to the original telephone survey. The survey
looked for adults with one of four mental illnesses. The only autistic
condition was Asperger syndrome but Brugha et al now claim to be able to give a
global figure for all autistic conditions which is of course impossible. Whilst
having research ethics approval the study was not carried out according to
accepted ethical standards. Informed consent was not obtained. Participants
were misled as to the purpose of the survey. They were not told they were being
assessed to ascertain if they were mentally ill. A financial inducement to take
part of a shopping voucher was offered – aside from ethical issues that would
tend to encourage those of lower incomes to participate and invalidate the
study. Mentally ill people are more likely to be of lower income if their
ability to earn a living is impaired.]"

And SBC was asked in 2009
where are all the "lost generation" 40-60 year-old non-verbal autistics wearing
diapers and banging their heads on walls and spinning around - but as is his
custom he has not had the decency to reply.

And the NHS is now in full
criminal deceit mode, with non-autistic non-disabled older people being falsely
given autistic diagnosis on the faintest excuse, whereas mothers of severely
disabled toddlers despair of getting any honest diagnosis - just to pretend the
increase has not happened, just as this deceiving "review" paper does too.

For these reasons Brugha's (and any similar studies)
amounts to no evidence whatsoever for countering the real evidence of
Hertz-Picciotto and others.

~~~~~~~~~~~~~~~~~~~~~

Letter signed for on 12th Jan (though not by SBC himself):

9th
January 2016

Dear
Dr Baron-Cohen,

I am
writing here in respect of your article "Identifying the lost
generation of adults with autism spectrum" in Lancet Psychiatry 2015.

I am
concerned that I have not yet heard from you about this article.I hope you are not unwell.

I
will send herewith a copy of my correspondence with your co-author Meng-Chuan
Lai.His replies get even more absurd
and indefensible than the original article (indeed raising doubt about his
sanity).This matter of the huge tragedy
of the manyfold increase of autism (and the outrageous claptrap such as Brugha
being used to pretend it hasn’t happened) is very serious.Publishing of sloppy, wantonly misleading
writing about it is completely unacceptable and unethical.It is all the more unacceptable that you
yourself put your name to such a grossly misleading and unworthy document,
given that you are widely trusted as “the leading expert” on autism.And further that this is the very opening of
a “review” being published in the Lancet no less, thus likely to be
“authoritatively” parrotted by future generations ofstudents as supposed established knowledge.

I
included two of your email addresses in my correspondence with Meng-Chuan (sb205@cam
and editorial@molecularaut)but have not heard any comment from yourself on the matter.I do not know whether you are aware or not
of these issues (though as co-author you should have been aware of the opening
sentences of your own article anyway).Accordingly I am now sending this letter by signed delivery requesting
that you clarify your position on this very important matter.Do you agree with myself and others that the
article is unacceptably misleading and must be retracted?Or what?

I
look forward to hearing from you as soon as practical.You have one of my email addresses at the
top here, and another is rpclarke@autism.

This review by Dr Meng-Chuan Lai
and Dr Simon Baron-Cohen (SBC) should be retracted for being outrageously misleading. It starts with an assertion of a highly dubious
massively important controversial “fact” with no citation whatsoever in
support.

The opening sentence (of both
abstract and text) asserts to us that as of 2014-15, 1% of 10-year-olds are
autistic, and 1% of 30-year-olds are autistic, 1% of 50-year-olds are autistic,
and so on, for “all ages”.And the
title of the paper reinforces that untruth with the notion that there is
therefore a “lost generation” of older autistics who have mostly remained
unrecognised as autistic and thus “lost”.The un-explicated implication being that there has not been any increase
of autism but instead only an increase of awareness or diagnosis.And this paper sets out from its beginning
by grossly misleading the reader into assuming that that is known to be a fact,
indeed established to such an extent it doesn’t even need any citation in
support.

And that title and first sentence
are not incidental to the paper but are its central premises.

I sent emails to the authors,
querying the justification for that first sentence.I got no reply from SBC.

Dr Lai sent a series of
replies.The full correspondence is too
lengthy to include here in full, but here are some main excerpts.

Dear Robin,

Thank you for your message. For clarification, when we write
“Autism spectrum conditions (panel 1) comprise a set of neurodevelopmental
syndromes with a population prevalence of 1% across all ages.” we are NOT
referring the term “ages” to different chronological years (i.e., 1970s, 80s,
90s, etc.) but are referring it to the ages of the individuals; that is, we are
referring to epidemiological evidences that recent cross-sectional studies in
children, in teenagers and in adults all tend to show a prevalence around 1%
(depending on studies but can range from around ~0.5% to ~2%). We, therefore,
have no intention to argue in the paper whether the prevalence of autism is
constant or not across different chronological years.

Hope this clarifies the question/mis-understanding.

Regards,

Meng-Chuan

Dear Meng-Chuan,

Thanks for your reply. Unfortunately it appears
to me to be completely bonkers. Your phrase “all ages” includes obviously
those who are 40 or 60 years old. And even older. As of 2015, a
person who is age 40 was necessarily born in 1975 or earlier, and a person of
age 60 was necessarily born in 1955 or earlier. That is, such ages of
persons are impossible to disentangle from the huge change of apparent
incidence (per birth-year cohorts) which is the basis of the notion of the
autism increase. I fail to see any way you can separate ages (of “all
ages”) from specific years of birth.

In response to my request for any evidence to support
that claim of your first sentence, you didn't send any, but instead included a
sentence contradicting it. And that notion of “1% across all ages” is
fundamental to the point of your entire article, namely the notion of a “lost
generation” of older autistics.

(If I may do a bit of your homework for you here,
perhaps the cited Brugha et al. could be supposed to constitute supporting
evidence on the matter. But Brugha et al. is fundamentally unsound.
They went to great lengths for establishing reliability of the
assessments. But no establishing of the (infinitely more important) validity
of the assessments, that is establishing that the measures at age x were
equivalent to the measures at age y. And that is because it is
logically impossible to do that validity verification (except maybe over many
years). It's a bit like if I put a steel ruler in a hot fire and declared
that I can see that its own scale shows it to be still exactly 12 inches
long, so “therefore” the heating hasn't changed its length. For this
reason Brugha's (and any similar studies) amounts to no evidence whatsoever for
countering the evidence of Hertz-Picciotto and others.)

But your present article is simply unacceptable
(seriously misleading) and has to be retracted.

Sincerely, Robin P Clarke

Dear Robin,

Thank you for the opportunity for further clarification. If
I understand your points correctly, the main critique is based on your
perception: "that notion of "1% across all ages" is
fundamental to the point of your entire article, namely the notion of a
"lost generation" of older autistics".

I am sorry if this is how you perceive our arguments.
However, this is not what we have in mind when we wrote it. You are right that
the paper mainly discusses under-recognized autism in adults - indeed the sole
focus of the review, and from a clinical perspective. We are asked by the
journal to provide general epidemiological background (based on published
studies), and this is where the ~1% number comes from - and we provided the
number in adults, referencing the Brugha paper which is one of the few
published study focusing on adults. We DO NOT mean to argue "there
is a constant 1% prevalence over the years so there is a lost generation".
We simply refer to the current epidemiological findings that adult prevalence
at the time being is also around 1%, and many of them have not been diagnosed
in the past. I agree it is difficult to get the ground truth (due to
issues with validity of diagnosis, changes of diagnostic concepts [that we have
discussed in the review], and not knowing whether there is true incidence
change); the prevalence number cited here is simply giving a general picture to
the readers, from available published epidemiological data.

It is possible that there is increased incidence over the
years, but this does not contradict the possibility of people being
under-recognized as a child. We focus on the latter and have no intention to
discuss (either support or refute) the former.

I hope this helps clarify where this review comes from.

Regards,

Meng-Chuan

Still not having heard anything from SBC himself, on 9th
January I posted a letter to him by Signed-For-Delivery (KP597377771GB at
royalmail.com) as follows.

Dear Dr Baron-Cohen,

I am writing here in
respect of your article "Identifying the lost generation of adults
with autism spectrum" in Lancet Psychiatry 2015.

I am concerned that I
have not yet heard from you about this article.I hope you are not unwell.

I will send herewith
a copy of my correspondence with your co-author Meng-Chuan Lai.His replies get even more absurd and
indefensible than the original article (indeed raising doubt about his sanity).This matter of the huge tragedy of the
manyfold increase of autism is very serious.Publishing of sloppy, wantonly misleading writing about it is completely
unacceptable and unethical.It is all
the more unacceptable that you yourself put your name to such a grossly
misleading and unworthy document, given that you are widely trusted as “the
leading expert” on autism.And further
that this is the very opening of a “review” being published in the Lancet no
less, thus likely to be “authoritatively” parrotted by future generations ofstudents as supposed established knowledge.

I included two of
your email addresses in my correspondence with Meng-Chuan (sb205@cam and
editorial@molecular)but have not
heard any comment from yourself on the matter.I do not know whether you are aware or not of these issues (though as
co-author you should have been aware of the opening sentences of your own
article anyway).

Accordingly I am now
sending this letter by signed delivery requesting that you clarify your
position on this very important matter.Do you agree with myself and others that the article is unacceptably
misleading and must be retracted?Or
what?

I look forward to
hearing from you as soon as practical.You have one of my email addresses at the top here, and another is
rpclarke@autism.

Sincerely, Robin P
Clarke

I have still not received any reply to this letter, by
email, post or any other means.Why
not?

“I have
only two questions for you:
1. [....]
2. [....] I'd like you to show us the 30, 50, and 70 year old
adults who display the same symptoms of classic autism that we see in
children, the non-verbal adults in diapers, banging holes in walls and spinning
in circles. [...]”

The reply from SBC went on quite a bit, but did not give the
slightest answer to those questions.Again, why not?

And this hugely misleading from SBC comes in a context of
his twice blocking my own evidence about the increase.When I sent to his Molecular Autism journal
my epidemics paper, he replied with an assertion that “The advice we have
received is that the methodology would not get through critical peer review
from our journal”.And yet this is a
pseudo-reason, because it is the editors themselves (i.e. himself) who choose
the peer reviewers and thereafter decide whether or not the peer reviewers have
shown the paper to be inadequate or not.

And a second occurrence of blocking by SBC occurred when I
sent to his journal my paper about road traffic pollution as a supposed cause
of autism.He refused to publish it
unless I cut out all mention of my alternative explanation (in terms of reduced
ventilation of the mercury vapour emitting from non-gamma-2 dental amalgams).

The purpose of this website is to provide material supplementary to the update review (not yet published) of the 1993-published autism theory paper (linked in header above). All the posts here serve that purpose in one way or another, but some are more worthwhile or necessary than others. So here is a brief guide to the contents here.

"Skeptical" people will generate plenty of supposedly clever reasons for rejecting the whole basis of the antiinnatia theory. That's despite the fact that any such "skeptics" must therefore be instead gullibly taking seriously one of a handful of utterly absurd alternative theories as explained in the update paper.

Autism research is now becoming seriously distorted by official charlatanism similar to that of which the proof is shown here. And that distortion directly affronts the truths to which this theory relates. One of the leading sources of extreme misinformation is the book by Paul Offit, which is being distributed free to parents of victims via the American Academy of Pediatrics.

The myths:

that there has been no autism increase,

that mercury is not associated with autism, and

that removal by chelation cannot help,

are all addressed in the articles linked above and therefrom (and more fully in conjunction with the update review paper).

You can find the link to the spectacularly-predicted Purgatorius video here, along with some further evidence relating to my explanation of the hand-flapping.

Some other peoples' excellent graphs of the increase in the US can be found here, particularly the ones with multiple differently-coloured curves. They basically confirm my interpretation of the California DDS data as essentially a simple exponential-shaped increase.

Mitochondrial dysfunctions could be caused by antiinnatia (both within and without the brain), or they could be a non-antiinnatia "side effect" of mercury toxication. They could be part of some processes whereby antiinnatia affects neuronal function. So the reports about mitochondria appear to give neither support nor challenge to antiinatia theory.

Data on a "photoninthedarkness" blog leads me now to thinking that the increase has involved some diagnostic substitution, but not in the way that is assumed by pro-vaxxers. More later, but I reckon when there was a rapid real increase of autism c. 1985-1995, much of it was incorrectly diagnosed as non-autistic retardation. Thereafter the diagnoses substituted to the correct autism diagnoses. This leads me to suspect that the autism increase actually stopped increasing about ten years ago and since then it's just been an artifact of substitution.

“We’re finding that the immune system seems to function at a lower level in autism,” says Hertz-Picciotto. Which could be because the dental mercury that caused the autism increase is well-known to also impair immune functioning.

1. The Abstract is misleading
as to what information this manuscript provides, stating that, "This is
the first-ever study of health consequences of non-gamma‑2." This is not a
"study," as usually defined, as no measurements of non‑gamma-2 were
made, nor were any health consequences assessed except population-level
statistics about prevalence of disability.

Three baseless pseudo-points in
one sentence there – I will chop it up for my replies.

>no measurements of
non-gamma-2 were made,

As my review stated, indeed,
no-one has ever bothered to keep records of the usage or prevalence of
non-gamma-2.Even my own dental
hospital records never recorded the different amalgam types (and I am aware
that I started off with the earlier crumbling “conventional” types and later
had the extremely durable non-gamma-2’s).

That lack of data is not a fault
of this work but rather a scandalous offence by those authorities who didn’t
bother to even keep records.However, a
confident inference can still be made that the overall amount of non-gamma-2 in
people’s mouths would have progressively increased as more and more of their
teeth were fitted with the new materials.This review thus provides the absolute best quantitative information
currently (and almost certainly ever) available.

>nor were any health
consequences assessed except population-level statistics about prevalence of
disability.

Again, that lack of data is not
a fault of this work but rather a scandalous offence by those authorities who
didn’t bother to even seek reports on possible adverse events from amalgam, but
instead implemented the cover-up measures documented in the paper.Which means those population-level
statistics are about as good as it can get.It does not follow that they are worthless, else quite a number of other
“not-really-studies” in very prestigious journals would also have to be
dismissed.

>This is not a "study", as usually defined,
as no measurements of non-gamma-2 were made, nor were any health consequences
assessed except population-level statistics about prevalence of disability.

Really?In that case there are numerous other papers
which were “not really a study”, despite being published in the most
prestigious journals and highly promoted as indeed being important “studies”.Their authors likewise didn’t do any
measurements or diagnoses but instead presented existing data as I have.These include for instance:

No-one has ever proposed that
any of those were not really studies.And that’s just a few I’ve come up with this minute.A more reasonable consideration of the
matter is as follows.Journals categorise
papers as either “reviews”, or “studies”, or something else such as
commentaries.But that categorisation
is rather crude, like categorising people as either “black” or “white”.In reality there is a fudging between two
notional ideal types, namely “proper reviews”, of which the input data consists
entirely of pre-existing published studies (of for instance whether walking
causes autism), and “proper studies”, in which the investigators do some
measuring either in a laboratory or out in the wider world.Those seven famous papers listed above fit
into neither of those ideal categories, just like this present one.But so what.There has never before been ANY scientific paper about the health
consequences of non-gamma-2 amalgams.And no-one has ever compiled any measurements into a published
study.It follows that it cannot be
either of those ideal types, but it does not follow that it cannot be an
excellent scientific paper any more than those seven above are not.In reality it is properly described as both
the first ever study of the known data, and as the first ever review of the
evidence.

2. P.4: Evidence needs to be provided for the
statement that “...Hal Huggings and other dentists were struck off the register
of practitioners.” for issuing warnings about the amount of mercury released
from non-gamma-2 amalgams.

Firstly, that point is far from
a key foundation for any conclusions of this review.I doubt whether it warrants taking up additional space on
documentation merely on the basis that some people might wish to not believe
it.Secondly here are some evidential
details of the matter which I have quickly dragged from the web:

3. P.5: The statement that, "Consequently, declining
rates of amalgam installation would conceal an increase of prevalence of the
amalgams in patients' mouths" is a non-sequitur. If fewer amalgams
are being placed, how could their prevalence increase? It might mean that this
trend would conceal an ongoing release of mercury vapor in the mouths of
individuals with such amalgams, but not the number of individuals with them.

Dear Reader, please go to your
kitchen sink, put the plug in firmly and water-tight, and then turn on the tap
to flow fairly fast, till an inch or two of water accumulates.Then turn the tap down so there’s only a
little more coming out per second.And
now you can see that the water level in the sink stops rising but instead
quickly goes down, as it must because the rate of additional input of the water
has decreased, so obviously the total amount in the sink must decrease
correspondingly.Or at least that is
presumably what happens in the kitchen of someone with enough scientific
expertise to judge such things.

For the educationally-deprived
among us I’ll go through that paragraph again, with tutorial hints added:

Dear Reader, please go to your
kitchen sink [analogous to patients’ mouths], put the plug in firmly and
water-tight [analogous to the fact that non-gamma-2s stay in those mouths for
whole lifetimes], and then turn on the tap [analogous to dentists installing
non-gamma-2s] to flow fairly fast, till an inch or two of water
accumulates.Then turn the tap down so
there’s only a little more coming out per second [analogous to “declining rates
of amalgam installation”].And now you
can see that the water level [analogous to the prevalence of the amalgams in
the mouths] in the sink stops rising [contrary to silly me’s expectations] but
instead quickly goes DOWN [well, highly-qualified expert Reviewer #1 apparently
thinks so, so there], as it must because the rate of additional input of the
water has decreased, so [“]obviously[”] the total amount in the sink must
decrease correspondingly.Or at least
that is presumably what happens in the kitchen of someone with enough
scientific expertise to judge such things.

I did emphasise in my review
that the whole point of non-gamma-2 was that they are far more durable
(indeed can easily last a whole lifetime).Just like that water which doesn’t suddenly start to rush out of the
sink just because you turned the tap down.

4. P.5: The author states
that information is not available on "usage or total prevalence of
non-gamma-2 in people's mouths." Given this, any statements made about the
health consequences must remain purely conjecture.

Firstly Reviewer #1 here
misrepresents what I wrote.I did not
state that “information is not available…”.My words were:

“I
have been unable to obtain any numerical data on usage or total prevalence of
non-gamma-2 in people’s mouths.The DH
have told me they have no such records.And NHS dental records have not recorded the types of amalgam used.It is unlikely that any better information
is available in other countries.But we
can very reasonably assume that the overall prevalence of non-gamma-2 will have
gradually, progressively increased in the decades following its introduction.”

And you can see there that I had
already pre-answered this half-baked objection.It is in the nature of reality that the prevalence of something must
inevitably increase for some period after its introduction as the new standard
product.And it is common knowledge
that people usually have their further tooth fillings put in in dribs and drabs
over the years so their prevalence will correspondingly increase over a period
of years rather than of minutes or millenia.Which is very much in line with those increase curves of autism, adult
disability, and later age of onset, which also occur over years following the
change to non-gamma-2.

.

5. P.6: The author states that he or she did not
"cherry-pick.. selected data to prove any point," yet that is done in
the last paragraph on this page, when reviews supporting the hypothesis that
mercury is etiologically involved in autism are cited, but reviews that
conclude that it is not are not cited.

But again, Reviewer #1’s
assertions are multiply untrue.Firstly, reviews are not data.Secondly, in that very section supposedly at fault here, I did
indeed explicitly cite the entire (supposed) counter-data, namely the three
studies which have been claimed to disprove the mercury-autism link, namely Ip
et al, Soden et al, and Hertz-Picciotto et al.So that instance asserted by Reviewer #1 shows the exact opposite of what
Reviewer #1 asserts.And thirdly, my statement
about not cherry-picking was only in my section headed “My epidemiological
investigations”, and specifically a comment about my own presentation of data
of the time-trends of autism, adult disability, and amalgams.What great contrary data have I omitted
there?In reality there has been not
the slighest cherry-picking and this is merely yet more nonsense from this
so-called peer reviewer.

6. P.7: The fact that mercury excretion is increased
following administration of DMSA in individuals with autism does not prove
much, as the action of DMSA is nonspecific. Excretion of other metals (lead,
antimony) is also increased.

Yet more cheap muddle from
Reviewer #1.The finding in Bradstreet
et al was not “The fact that mercury excretion is increased following
administration of DMSA in individuals with autism”.Rather it was the finding of a major difference between
autistics and non-autistics, with the autistics outputting three times as much
mercury as the non-autistics (with fluke probability of 1 in 5000). AS
ALREADY CLEARLY STATED RIGHT THERE.Did this faceless reviewer cheat to get their PhD too?

7. P.7: The conclusions of the Holmes et al. (2003) study
are weak, not because of whatever biases the investigators might or might not
have but because the findings are not credible. In this study, the mean mercury
level in the hair of controls was 3.63 ppm, which is much higher than would be
expected in a representative sample of infants. By comparison,
measurements of mercury in children's hair in an NHANES survey conducted about
the same time (1999-2000) (McDowell et al., Environ Health Perspect
2004;112(11):1165-1171) reported a mean of 0.12 ppm (and 0.16 among
fish-consuming children). This suggests that the controls included in the
Holmes et al. study were biased with regard to their mercury status and that an
8-fold reduction reported in the hair mercury level of "autistic
cases" is likely an artifact.

Here Reviewer #1 shows a bit
less incompetence, and stumbles only in terms of a rather more subtle
fallacy.We could call it “the fallacy
of the assumed all other things being equal”.A good other example of it is found in various comments about the
Hallmayer et al 2011 twin study finding of autism being mainly
environmental.Commenters on Hallmayer
et al have concluded that it shows that the earlier twin studies were
“wrong”.But well, they “must be wrong”
mustn’t they?, because Hallmayer et al is a big powerful new study and so it
must trump those little old ones into the wastebin of “wrong” results.

The
fallacy here is the unfounded assumption that all other things are equal
(constant).In respect of those twin
studies, please have a look at my still-unchallenged paper “A theory of
general impairment of gene-expression manifesting as autism”, which appeared in
print in 1993 and is still essential reading for anyone who wants to have a
clue about the subject.Therein I
specified the conditions under which autism would change from a mainly genetic
condition to mainly environmental: “If a rare perinatal
adversity were to become somewhat more common, then obviously, autism of the
environmental category would become more prevalent.”And now with the huge impact of
non-gamma-2 in parents’ and carers’ mouths, exactly such a condition has indeed
occurred, and so hardly surprisingly the causation of autism has indeed CHANGED
from mainly genetic to mainly environmental.There is no real conflict between Hallmayer and the earlier twin
studies, merely differences of the underlying and unexamined variables.Likewise, in respect of mercury and autism
we know that there is a lot we do not know.You can see in my own review section there how the various studies of
autistic hair give divergent results and that there is nevertheless good reason
to find them all valid and true.Likewise, to dismiss the Holmes et al result as “not credible” just
because of those non-standard levels entails an unwarranted gross presumption
that there are no important unknowns going on between the different
studies.And so the finding of Holmes
et al should not be dismissed unless there is a more substantial basis for
doing so.And on the contrary, later
studies have supported their ‘perverse’ data of lower hair mercury levels in
autism.This Reviewer #1 is here categorising
the careful work of Holmes et al as {either grossly incompetent or grossly
fraudulent}, on a basis of no real evidence but merely because he/she does not
find their results in accordance with the required
commercially/professionally-convenient dogma.

> I don't think it is appropriate to state that a
pattern of findings provides any evidence as to whether an investigator was
"acting competently and honestly."

Whereas I do think it
appropriate.And that is because
fraudsters or incompetents are extremely unlikely to come out with a whopping
strong result that is:

(1) markedly contrary to what
they would have expected;

(2) markedly contrary to what
they would have found convenient to report; and

(3) only subsequently supported
by the collection of results of later other-people’s studies of autistic
hair mercury.

And in the context that many
have presumed to shallowly discredit Holmes et al as either incompetent or
fraudulent (as Reviewer #1 here does him/herself), that consideration is
outstandingly eminently appropriate to be stated.

8. P.7: The author multiplies
the P-values from 6 studies to calculate the probability that the findings are
due to chance. This is a meaningless calculation. First, the studies included
reached different conclusions about the hair mercury levels of children with
and without autism (although the author argues that age needs to be taken into
account). Second, given that all P-values are less than 1, multiplying them
necessarily results in a smaller and smaller number the more studies one
includes. If each of the 6 studies yielded a P-value of 0.5 (indicating
no statistically significant relationship), then using the author's method, the
combined P-value would be 0.0156, which would suggest that, in aggregate, the
studies provide significant evidence of an association. Third, even if the
author's method was valid, it would be necessary to include in the calculation
all of the studies ever conducted of a particular hypothesis, not just those
selected because they purport to show an association (just as it is necessary,
in a meta-analysis, to include all available evidence).

Again I shall
have to chop the above into shorter bits for reply, as follows.

>The
author multiplies the P-values from 6 studies to calculate the probability that
the findings are due to chance. This is a meaningless calculation.

(It is absolutely standard
probability maths to multiply together probabilities to get the compound
probability of them all happening merely by fluke, as any betting shop can
confirm, but we must continue here with Reviewer #1’s further exposition on
this point…...)

>Firstly, the studies
included reached different conclusions about the hair mercury levels of
children with and without autism (although the author argues that age needs to
be taken into account).

This misrepresents the
situation.I don’t “argue” that age
needs to be taken into account, rather I observe that age needs to be
taken into account, in that the earlier ages always give lower mercury in
autistics, while the later ages always give higher mercury.Thus none of those studies are in any
conflict with the reasonable hypothesis mentioned by Majewska et al that the
adrenarche plays a role in the hair mercury levels.There is therefore not any real conflict between these studies
but rather voices declaring in common that mercury is involved in autism in
some way.(And Reviewer #1 is here
again employing that fallacy of the presumed all other things being equal – age
in this case.)And so there is no valid
ground there for not multiplying together those probabilities.

>Secondly, given that all
P-values are less than 1, multiplying them necessarily results in a smaller and
smaller number the more studies one includes.

That is of course true. [Note
for non-expert readers: smaller P-values indicate the results are less likely
to be mere flukes and so are more “significant”.]

>If each of the 6 studies
yielded a P-value of 0.5 (indicating no statistically significant
relationship), then using the author's method, the combined P-value would be
0.0156, which would suggest that, in aggregate, the studies provide significant
evidence of an association.

And that is also indeed
true.But so what.It is indeed the reality that several bits
of weak evidence can add up to strong evidence.Indeed that is the whole point of making a (for instance
clinical) study large enough to give a significant result.Any such study can be conceived of as being
a combining together of lots of smaller sub-studies, any one of which could
give non-significant results, but when all put together would enable a highly
significant result.And that high
significance is not some specious false result, rather it is the entirely sound
statistical inference.And that’s what
I’ve done there, except that my p values were all highly significant
already.And the fact that the
evidence there is of diverse types adds all the more to its methodological
robustness, as it is not wholly founded on any one premise.

>Thirdly, even if the
author's method were valid, it would be necessary to include in the calculation
all of the studies ever conducted of a particular hypothesis, not just those
selected because they purport to show an association (just as it is necessary,
in a meta-analysis, to include all available evidence).

Again, not so.Firstly, there IS no contrary evidence on
the mercury-autism question such as could make any meaningful reduction of my
combined calculation.I’ve pointed out that
even the three supposedly counter results were actually pro in reality.Secondly, I made the point that that is the
probability only from those few studies combined.It logically follows that if there were more studies, and
continuing on the same 100% positive connection trend, then that would simply make
my big fluke number even bigger (smaller).So there is still no sound objection to my probability calculation.

9. P.8: The argument about the evidentiary value of never
having seen the Queen is a little ridiculous and, in my view, has things
completely backwards. It is by means of the falsification of hypotheses that
science advances. A single negative result is enough to call into
question a positive result that has repeatedly been observed and might be the
result of bias (all it takes is the observation of one black swan to refute the
statement that, "all swans are white"), but no number of positive
observations is sufficient to demonstrate the universality of a statement.

Again I will need to chop this
up for my replies.

>9. P.8: The argument about the evidentiary value of
never having seen the Queen is a little ridiculous and, in my view, has things
completely backwards.

As we’ll see in the next
few lines…(?)

.

>It is by means of the falsification of hypotheses that science
advances.

Partly so, but also there cannot be any advance at
all if hypotheses are prevented from being properly raised in the first place.
And Reviewer #1 is doing a great job of preventing some very important
hypotheses being raised, via these unflattering would-be-critiques right here.

>A single negative result is enough to call into
question a positive result that has repeatedly been observed and might be the
result of bias (all it takes is the observation of one black swan to refute the
statement that, "all swans are white"), but no number of positive
observations is sufficient to demonstrate the universality of a statement.

Reviewer #1 here uses
some extremely incompetent language to confuse the matter.Namely the notion of a “negative
result”.For example an investigation
of whether or not the Queen actually exists could come up with two very
different types of results, both of which Reviewer #1 would have us class as
“negative results”.On the one hand,
there could be a failure to see the Queen on peeping over the palace wall; on
the other hand there could be a finding of the absence of the Queen anywhere in
the UK following an insanely.detailed mega-search from South to North and
back.The difference between a
“negative” failure to find something and a (positive) finding that that
something is actually absent, is complete and absolute, and not to be confused
by conflating into a false notion of “negative results”.

>A single negative result is enough to call into
question a positive result that has repeatedly been observed and might be the
result of bias

I shall here now correct
Reviewer #1’s grossly incompetent language.

“A single FINDING OF
POSITIVELY CONTRARY evidence is enough to call into question THE UNIVERSALITY
OF [an earlier] result that has repeatedly been observed and might be the
result of bias.”

“A billion mere
FAILURE-TO-FIND results CAN BE STILL NOT enough to call into question [an
earlier] result that has repeatedly been observed and might be the result of
bias.”

When I used the words
”negative results” it was self-evident from the context that I could only mean
the latter, more common meaning of the term, and not the “positively contrary”
meaning.But Reviewer #1 still managed
to muddle it as ever.

10. P.8: The discussion of
the validity of the three studies sometimes described as refuting an
autism-mercury link requires fleshing out. It is necessary to tell the
reader the arithmetic error Ip et al. made and to demonstrate the extent to
which it altered the study conclusions. The reader is told that DeSoto and
Hitlan (2010) concluded that Soden's study "actually proved the
opposite," but no information is provided that would enable the reader to
evaluate this statement. The conclusions of Hertz-Piccioto et al. are
misstated. The second-to-last sentence of this paper actually states,
"This report did not address the role of prenatal or early-life Hg
exposure in the etiology of autism." The major finding was that
total Hg in blood was not elevated or reduced in preschool children with
autism/ASD compared with unaffected controls and resembled those of a
nationally representative sample. The reason for the authors'
qualification is that only concurrent measures of blood Hg were available,
meaning that they could draw no conclusions from their data about the role of
prenatal or early-life mercury exposure. To say that the authors
concluded that their data, ".constituted no evidence whatsoever against
causation of autism by mercury" is simply wrong.

Again, I need to chop this up
for my replies.

>10. P.8: The discussion of the validity of the three
studies sometimes described as refuting an autism-mercury link requires
fleshing out.

….because…..

>It is necessary to tell the reader the arithmetic
error Ip et al. made and to demonstrate the extent to which it altered the
study conclusions.

Really?I cited the conclusion of DeSoto and Hitlan
(2010) that the study actually proved the opposite.(Ip et al was retracted due to their major but elementary
error.)On this question this reviewer
should either explain why D&H were wrong or else shut up.Here’s what they said:

“The author of record has publicly acknowledged that
these numbers and the statistical calculation were in error in an erratum (Ip
et al. 2007) and the journal editor notes the reason given was a series of
typographical errors (Brumback 2007). Furthermore, a careful and correct
analysis of the full data set results in a statistically significant difference
(Brumback 2007, DeSoto and Hitlan 2007, DeSoto 2008) with autistic children
having higher mean levels of mercury.As can be seen by comparing the erratum to the original article, the
standard deviations were wrong for both groups, the stated statistical
significance in 2004 was not even close: their original stated level of
statistical probability was off by almost 10 fold.”

>The reader is told that DeSoto and Hitlan (2010)
concluded that Soden's study "actually proved the opposite," but no
information is provided that would enable the reader to evaluate this
statement.

Not so.I provided the citation of D&H along
with the citation of the original Soden, which is all the information that is
needed for that evaluation.If Reviewer
#1 reckons there is something wrong with D&H’s conclusions then he/she
should state what it is, or else shut up.Here’s what D&H said:

“In
the end, the statistical test conducted by Soden and coworkers is meaningless
and distracting from the essentials of what was done. The authors measured
metal levels, then (based on the lab definition of toxicity) all values were
defined as zero, then – they tested this actual zero statistically and found
that one could not rule out zero. “

“But
let readers be clear about this central point: if one is willing to consider
the actual numbers reported and test those numbers, the results are clear - a
larger proportion of autistics had heavy metals excreted as the result of
chelation.”

It is not the business of
authors of papers to have to recite the details of all the prior papers they
cite in support; if they did there would be even more that everyone had to
read.Any half-proper peer reviewer
would check out the background references themselves (where required), and
indeed in this case ought to be an expert familiar with these important key
papers (on Neurotoxicology of autism) already anyway.What a timewasting pseudo-expert charlatan.

>The conclusions of
Hertz-Piccioto et al. are misstated.

Not so.They are not in the slightest mis-stated in
my own report.

>The second-to-last sentence of [their] paper actually
states, "This report did not address the role of prenatal or early-life Hg
exposure in the etiology of autism."

Indeed that is the case. But so
what?That is exactly my point about
it. [Note to non-expert readers:“Hg”
means mercury and “etiology” means causation.You may wish to guess whether they used that unnecessarily abstruse
language there for the same reason that they hid that absolutely crucial sentence
right at the end, second last, of their paper which supposedly did indeed dis-evidence
a mercury-autism connection.]

>The major finding was that total Hg in blood was not
elevated or reduced in preschool children with autism/ASD compared with unaffected
controls and resembled those of a nationally representative sample.

Indeed that is the case.But so what?I never said otherwise.

>The reason for the authors' qualification is that
only concurrent measures of blood Hg were available, meaning that they could
draw no conclusions from their data about the role of prenatal or early-life
mercury exposure.

Indeed that is the case. But so
what?That is exactly my point about
it.

>To say that the authors
concluded that their data, ".constituted no evidence whatsoever against
causation of autism by mercury" is simply wrong.

No it isn’t.Their words quoted above
indicate PRECISELY that.As Reviewer #1
appears to be having some peculiar difficulty with either language or logic I
will try to parse this for them as follows.( I apologise that I have to assume the reader is an idiot here.)

We begin with their paper’s
second-last sentence that:

"This report did not
address the role of prenatal or early-life Hg exposure in the etiology of
autism."

That means effectively the same
as:

"This report was not
capable of providing any information about the role of prenatal or
early-life Hg exposure in the etiology of autism."

Which means that it is also the
case that:

"This report did not
provide any information about the role of prenatal or early-life Hg
exposure in the etiology of autism."

And hence:

"This report did not
provide any evidence about the role of prenatal or early-life Hg
exposure in the etiology of autism."

And hence:

"This report did not provide
any evidence about the role of prenatal or early-life Hg exposure in the causation
of autism."

And hence:

"This report did not
provide any evidence about the role of prenatal or early-life mercury
exposure in the causation of autism."

And hence:

"This report did not
provide any evidence about the causation of autism by prenatal or early-life
mercury exposure."

And hence:

"This report did not
provide any evidence against the causation of autism by prenatal or
early-life mercury exposure."

And hence:

"This report constituted
no evidence against the causation of autism by prenatal or early-life
mercury exposure."

And hence on merely removing a
redundant word:

"This report constituted no
evidence against [the] causation of autism by prenatal or
early-life mercury."

….which would be identical to my
own statement except that there is that extra bit about “prenatal or
early-life”.

So I was wrong there.I overlooked that autism could still be not
caused by exposure to mercury later in life, after that person has already
become autistic.So we’d best not
publish my non-gamma-2 rubbish after all.

And whatever it takes to become
a reviewer for Neurotoxicology, it’s all too clear I don’t have it
myself.

Reviewer
#2:

Dental amalgams are a
continual source of controversy. The current review attempts to survey the
adverse health consequences of the amalgam formulation known as non-gamma-2. It
asserts that these restorations "are currently by far the main cause
of chronic disability in the UK, US, and other such countries, with about 10%
of the UK working-age population disabled thereby." It also claims that
its introduction led to a 10-fold increase in the incidence of autism.

Indeed.But no faults are there providing basis for
non-publication so far.

As a contribution to this specialized journal, the
manuscript lacks any clear connection. It offers no neuro-mechanistic
foundation for such a correlation, especially for autism, which is a product
of disordered early development.

Not so.In respect of autism, my
review(/study/rant/) ties in the newer mercury factual data with the prior
unchallenged theory and the related fact of how the mercury binds with DNA to
reduce gene-expression and hence [as my 1993 had predicted] cause autism.And meanwhile in respect of adult mercury
poisoning there is quite a developed understanding of how the symptoms are
caused.The details of that causality
are in the cited literature or secondarily-cited.

It doesn't attempt to demonstrate any kind of
dose-response relationship.

No data is available that would
enable that.But it doesn’t follow that
there is no other useful evidence presented.

Its definition of autism lacks specificity.

It doesn’t need to.It just uses the definitions that are used
as standard by others. Asis common practice.

In addition, the claim that this amalgam formulation
accounts for 10% of chronic disability requires advanced statistical modeling
of exposure-consequence relationships in which other kinds of exposures are
concurrently evaluated.

Firstly, I did not claim that it
accounts for 10% of chronic disability.I reckoned from the data that it now actually accounts for MOST chronic
disability (something like 70-90%).That 10% figure was my estimate that wholly 10% of the UK workforce has
been disabled by non-gamma-2 (4 million victims out of a 40 million
workforce).

That 10% is not a “claim” but
rather was expressly only a rough estimate, from looking at figure 5.You can see that it shows an increase of
about 2 million accepted claimants, easily all attributable to
non-gamma-2.And you can see that it
peculiarly levels off about year 2000 as would be expected from the stated
political agenda of “claimant count now controlled”.And you can see that otherwise it would most likely have
continued upward to something like 4 million – hence 10% of the working-age
population.

And no fancy statistical
modelling is required to understand what these graphs are showing us.Of course they are not absolute proof, but
neither are they any lack of evidence, else we’d have to retract an amazing lot
of highly-acclaimed “studies” from the most prestigious journals.

In the absence of these kinds of information, it is
difficult to see how this manuscript is compatible with the aims and audience
of this journal. Perhaps the author should consider another kind of journal and
audience.

Or perhaps instead the so-called
Neurotoxicology journal should consider changing those aims and
audience, or perhaps change its name to reflect its “specialised” nature, for
instance to Specialised Neurotoxicology, Pedantic Neurotoxicology,
or best of all to Die Zeitschrift der Lysenkoischen
MeisterNeuroToxikologisten von Nurnberg (The Journal of the Lysenkoist
MasterNeurotoxicologists of Nuremburg).

Reviewer #3: This is an opinion piece on the possible role of mercury
exposure in the causation of autism.

Not so.It is not “an opinion piece”.Like all scientific papers it does include
proposed conclusions which are necessarily of an opinion nature.But for the most part it consists of
presentation of data and reasoning thereon, which is entirely in line with any
normal scientific paper and not “an opinion piece”.

The author makes a very impassioned case for non-gamma-2
amalgam fillings being the major cause for the rise in incidence of autism
using ecological data from UK, US and few other countries.

Not so.It is not at all “very impassioned” but
rather “very filled with as much useful factual evidence as can be found”.

No primary research has been undertaken by the author to
test this hypothesis.

So what.Exactly the same could be said about all
those seven highly-rated studies listed on the first page here.Has anyone ever called for their retraction
yet?

My main concern with this work is that it is not an
objective assessment of the evidence available at present.

….because / for instance…..

Key statements that form the basis for the author's
argument are unsupported by high-quality evidence.

…such as….

For example, the exposure of children to mercury from
their parents' amalgam restorations needs to be confirmed before the author can
make such a far-reaching conclusion.

Indeed, no one has bothered to
do any measurement studies of this question to date.But that is not the fault of this author or this review.Rather it highlights the urgent need to make
a start by publishing this first study of the subject, which can be then
followed up by testing studies.But I
did already explain why we can be confident that there is enhanced
exposure.That is because there is very
low background atmospheric mercury vapor, and it is known to constantly emit
from parents’ and carers’ amalgams, and they commonly spend much time together
with babies in enclosed spaces, even talking at them through their amalgam-filled
mouths, and so it logically follows that many babies are going to breathe in an
increased amount of mercury vapor at least on average.[Studies have also shown prenatal
transmission.]

Those two studies have already
been solidly debunked as evidence, as I pointed out via my first page citation
of Muttter 2010 (and others).Not least
they started too old to relate to causation of autism, and they stopped too
young to relate to causation of adult disability.In fact (as in my earlier journal replies) if I myself had been
in those studies I would have been recorded as evidence of harmlessness,
because my life only became chronically ruined (by the amalgam scam) AFTER the
age at which those propaganda studies stopped.And an editorial in the very same issue of the journal stated that those
two studies did not constitute evidence of amalgam safety. Why didn’t Reviewer
#3 mention that counter-point in their “unbiased” commentary here?

In fact, Maserejian et al. 2012 have reported that
compared to amalgam restorations, children receiving composite (non-mercury)
fillings showed impaired psychosocial function. There are several other such
instances in the manuscript where important data have been ignored.

Maserejian et al had not been
published when I first sent this review to a journal in July 2012, else I might
have mentioned it.But exactly the same
methodological problems arise as with the two others cited above.I myself was doing fantastically well at school
before the effects of the amalgam scam imposed themselves so devastatingly on
my life.And perhaps bisphenol-A might
well have injurious effects but that is a separate matter out of the range of
my own documents.

In my opinion, this
manuscript does not add unbiased scientific knowledge to the topic of mercury
and autism, and I cannot support it being published.

But rather it is this Reviewer who is biased, and has raised only bogus reasons
for suppressing the publication of this outstandingly important cautionary
information.

IN CONCLUSION:

These three reviewers have failed
to raise even a single sound reason for preventing the publication of this very
important information.And they have
meanwhile deployed a whole load of shallow pseudo-objections, which raises
considerable questions about both their supposedly expert competence and their
honesty.

And that comes in the context of
ten previous journals likewise raising only specious excuses for refusing
publication.

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Further reply from PseudoNeurotoxicology (23rd October 2013).

“…. Thank you for
your email. I forwarded it to the editor of the journal. After
review it was concluded that your manuscript was handled appropriately and the
original decision stands…..”

One of the few autism research institutions that are not in Lysenkoist denial about the increase of autism, the involvement of mercury, and the reality of sometimes recoveries, is the Autism Research Institute.

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